Abstract

Increased plasma renin activity in a hypertensive patient often provides an explanation for the mechanism of the hypertension and a clue to its origin. The mechanism is frequently that of vasoconstriction effected by the renin-angiotension system which originates in the kidney. No explanation or clue is offered in the hypertensive patient by a low plasma renin activity and its subnormal response to upright posture and sodium deprivation. Unlike<i>hyper</i>reninemia,<i>hypo</i>reninemia in this case implies no known mechanism, only an association that needs explaining. A small minority of hypertensive patients with low plasma renin activity have aldosteronism, in which renin release is suppressed by the negative feedback effect of excessive aldosterone. The latter, however, is normal in the majority of hyporeninemic patients. How, then, are we to explain the low renin activity and to interpret its theoretical and practical implications? Because about 25% of all patients with essential hypertension

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